This document discusses CT imaging findings of cerebral ischemia and infarction at different stages. It begins with an overview of the major types of stroke and their causes. It then discusses the pathophysiology of cerebral ischemia and infarction, highlighting the central ischemic focus and less dense ischemic penumbra. Next, it details the imaging appearance of acute, subacute, and chronic infarcts on CT. It notes the hyperdense artery sign seen in some acute infarcts. For subacute infarcts, it describes increased mass effect and hemorrhagic transformation seen 1-7 days later. It also briefly discusses lacunar infarcts and hypoxic-ischemic encephalopathy.

1. CT Imaging of Cerebral Ischemia and Infarction Presented by EKKASIT SRITHAMMASIT, MD. Ann G.Osborn Diagnostic Neuroradiology; 11: 341-369

2. Introduction Stroke is a lay term that encompasses a heterogeneous group of cerebrovascular disorders . The four major types of stroke : Cerebral infarction (80%) Primary intracranial hemorrhage (15%) Nontraumatic subarachnoid hemorrhage (5%) Miscellaneous – vein occlusion (1%)

3. Cerebral Infarction Large vessel occlusions ( ICA, MCA, PCA) – 40-50% Small vessel (lacunar) infarcts – 25% Cardiac emboli – 15% Blood disorders – 5% Nonatheromatous occlusions – 5%

4. Table of content Pathophysiology CT Imaging of Cerebral Infarcts: Overview Acute Infarcts Subacute Infarcts Chronic Infarcts Lacunar Infarcts Hypoxic-Ischemic Encephalopathy

5. Pathophysiology

6. Physiology of cerebral ischemia and infarction **Most common situation** Densely ischemic central focus Less densely ischemic “penumbra”

7. Physiology of cerebral ischemia and infarction

8. Physiology of cerebral ischemia and infarction **Ischemia produces** Biochemical Reactions Loss of ion homeostasis, Osmotically obligated water, anaerobic glucolysis Loss cell membrane function & Cytoskeletal integrity Cell death

9. Physiology of cerebral ischemia and infarction **Selective vulnerability** Most vulnerable = Neuron Follow by Astrocytes, oligodendroglia, microglia and endothelial cells

10. Physiology of cerebral ischemia and infarction **Collateral supply** Dual or even triple interdigitating supply : Subcortical white matter U-fiber, external capsule, claustrum Short arterioles from a single sourec : The cortex Large, long, single source vessels : Thalamus, basal ganglia, centrum semiovale

11. Physiology of cerebral ischemia and infarction Border zones / Vascular watershed Arterial perfusion pressure is lowest in these zone because of arteriolar aborization The first to suffer ischemia and infarction during generalized systemic hypotension

12. Border zones / Vascular watershed Adult, term infants Fetus, preterm infant Cortex and cerebellum Deep periventricular region

13. CT Imaging of Cerebral Infarcts

14. CT Imaging of Cerebral Infarcts The imaging manifestations of cerebral ischemia vary significantly with time

15. Acute Infarcts

16. Acute Infarcts The role of immediate CT in the management of acute cerebral infarction is two fold Diagnose or exclude intracerebral hemorhage Identify the presence of an underlying structural lesion such as tumor, vascular malformation.

17. Acute Infarcts First 12 hours Almost 60 % = Normal Hyperdense artery (25 – 50%) Obscuration of lentiform nuclei 12 – 24 hours Loss of gray-white interfaces ( insular ribbon sign) Sulcal effacement

18. Acute Infarcts Hyperdense artery Usually the MCA – hyperdense MCA sign (25% of unselected acute infarct) Hyperdense MCA sign 35-50% of MCA stroke Caused by acute intraluminal thrombus

19. Acute Infarcts Hyperdense MCA

20. Acute Infarcts Obscuration of lentiform nuclei

21. Acute Infarcts Loss of gray-white interfaces ( insular ribbon sign)

22. Acute Infarcts Sulcal effacement

23. Subacute Infarcts

24. Subacute Infarcts 1-3 days Increase mass effect Wedge-shaped low density area that involves both gray and white matter Hemorrhagic transformation (basal ganglia and cortex are common sites) 4-7 days Gyral enhancement Mass effect, edema persist

25. Subacute Infarcts

26. Subacute Infarcts

27. Subacute Infarcts

28. Subacute Infarcts ECCT

30. Chronic Infarcts

31. Chronic Infarcts Months to years Encepholomalacic change, volume loss Calcification rare

32. Chronic Infarcts

33. Lacunar Infarcts

34. Lacunar Infarcts Small deep cerebral infarcts Typically located in the basal ganglia and thalamus Small infarcts are often multiple Most true lacunar infarcts are not seen on CT Present they are usually seen as part of more extensive white matter disease

35. Lacunar Infarcts

36. Lacunar Infarcts

37. Hypoxic-Ischemic Encephalopathy

38. Hypoxic-Ischemic Encephalopathy Consequence of global perfusion or oxygenation disturbance Common causes – severe prolonged hypotension, cardiac arrest with successful resuscitation, profound neonatal asphyxia, cabonmonxide inhalation ( Decrease CBF) May be caused by RBC oxygenation is faulty Two basic patterns: “border zone infarcts” and “generalized cortical necrosis”

40. Border zones / Vascular watershed Adult, term infants Fetus, preterm infant Cortex and cerebellum Deep periventricular region

41. Hypoxic-Ischemic Encephalopathy The most frequently and severely affected area is the parietooccipital region at the confluence between the ACA, MCA, and PCA territories. The basal ganglia are also common sites In premature infants HIE manifestations are those of periventricular leukomalacia Most common observed on NECT is a low density band at the interface between major vascular territories. The basal ganglia and parasagittal areas are the most frequent sites.

46. At 2 months of age, T1-weighted brain MR imaging shows high - signal regions in the periventricular area, atrophy of the white matter and serrated ventricular walls .